Biological communication (the possibility for a cell to recognize a molecule or another cell) is a central phenomenon in pathological as well as in normal states.
Among the various mechanisms of molecular recognition between cells, and/or between cells and molecules, the binding of specific glycosidic structures by specialized proteins (lectins) is today considered as a major molecular recognition system.
The lectins may be bound specifically and non-covalently to well-defined glycosidic sequences.
Some lectins are bound, for example, to oligosaccharides which contain elevated mannose amounts, to structures carrying sialic acids, or to fucosylated glycosides.
Other lectins can bind .beta.-galactosides and lactose.
Multigeneric coaggregations exist between oral bacterial cells (such as Actinomyces naeslundii or viscosus, Streptococcus mitis or sanguis, Fusobacterium nucleatum, Porphyromonas gingivalis, Bacteriodes intermedius, etc.) which aggregate and form a network as the dental plaque.
Between these bacterial cells, the interaction is often obtained by a non-covalent bond between a .beta.-galactoside lectin on one cell and a glycosidic receptor on another cell (ref. 1).
Most infectious diseases are initiated by the adhesion of pathogenics agents (such as Actinomyces naeslundii, Fusobacterium nucleatum, Bacteriodes intermedius, Salmonella typhimurium, Vibrio Cholera, Campylobacter jejuni, Bacteriodes, Fusobacteria, Clostridia, Shigella, Yersinia, and Helicobacter pylori, etc.) to the epithelial cells of the mucosa of its host, which allows then the colonisation of the animal tissues.
This adhesion is often obtained by a binding between a .beta.-galactoside lectin located at the surface of this pathogeneous agent and a glycosidic receptor located at the surface of the epithelial cell (ref. 2).
Various cells of the immune system (lymphocytes T and B. macrophages, neutrophils) are known either to be able to bind .beta.-galactoside lectins or to express at their surface such lectins of the galectin family.
In addition, some epithelial cells such as intestinal cells or keratinocytes produce these galectins which can also coat Langerhans cells, and immunoglobulins such as IgE can specifically bind to galectins (ref. 3, 4 and 5).